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Delay in the maturation of muscle fibers in infants with congenital hypotonia.

Muscle biopsies of hypotonic children have shown delayed maturation of a fetal type of muscle fibers: subsarcolemmal halo devoid of activity for mitochondrial dehydrogenases, type II predominance and in some cases abnormal dispersion of fiber diameter. Fiber subtypes within group II were also abnormal. One case has definite embryonic characteristics with presence of myoblasts. Not a single clinical pattern was present in these patients and a variety of associated disorders were recognized. Some patients had a clinical picture corresponding to congenital benign hypotonia as described by Walton.

Child, Preschool

Targeted long-read genomic and epigenomic profiling enhances timely comprehensive variant discovery in hypotonia and muscle weakness.

BACKGROUND: Identifying the genetic basis of hypotonia and muscle weakness is critical for patient management and family counseling. However, diagnosis is often hindered by diverse genomic alterations, including repeat expansions, structural variants (SVs), and methylation defects. Standard-of-care testing, largely based on short-read sequencing, is limited in its ability to detect this heterogeneous variation landscape, leaving many patients undiagnosed or requiring lengthy sequential testing. Long-read sequencing represents a promising solution. However, its application as a first-tier diagnostic assay for hypotonia remains unexplored. METHODS: We retrospectively analyzed 227 patients with hypotonia to assess diagnostic yield, time-to-diagnosis, and costs associated with standard-of-care testing. A long-read whole-genome sequencing (LR-WGS) workflow with targeted analysis of hypotonia-associated genes was developed to detect and prioritize pathogenic SNVs, SVs, and CNVs, repeat expansions, and methylation changes at key disease loci. The workflow was validated in a reference-positive cohort with known diagnoses (n = 15) and applied to an unsolved cohort (n = 14). Variant interpretation followed ACMG guidelines and was confirmed with orthogonal methods. RESULTS: Standard-of-care testing achieved a diagnostic yield of 42% with an average time-to-diagnosis of 68.7 days; however, 30% of diagnosed patients experienced significant delays (average 169 days) due to sequential testing. The LR-WGS based approach identified all known pathogenic variants in the positive cohort, including SMN1 deletions, methylation defects at 15q11.2/Prader-Willi locus, FMR1 repeat expansions, and sequence and copy-number variants in > 100 genes underlying myopathies and muscular dystrophies. The targeted long-read pipeline reduced prioritized variant calls by 97.9-99.9% and, in the unsolved cohort, yielded one definitive diagnosis (de novo COL6A3 deletion) and one possible diagnosis (aberrant methylation and copy number at POMK), for an additional 14% yield. Among patients diagnosed after sequential testing (n = 29), LR-WGS is expected to reduce time-to-diagnosis by ~ 85% and decrease cumulative diagnostic delays, with projected healthcare cost savings of $396,000-439,000. Across the entire 227 patient cohort, LR-WGS is anticipated to reduce testing costs by 6.5%, yielding an average savings of $105 per patient. CONCLUSIONS: LR-WGS enables comprehensive discovery of genomic and epigenomic variants in hypotonia and muscle weakness, improving diagnostic yield, shortening diagnostic timelines, and reducing costs compared with current standard-of-care testing.

Humans

A case of Ullrich's disease (Kongenitale, Atonisch-Sklerotische Muskeldystrophie).

An unique myopathy described by Ullrich in 1930 was reported in a 4-year-old Japanese boy. Major clinical findings included proximal joint contracture, muscle hypotonia, prominent calcaneus, high-arched palate, and normal intelli gence. Muscle biopsy showed rather small muscle fivers with variations in size and proliferation of connective tissue. A review of 15 cases in the literature revealed this type of myopathy as a distinctive entity to be classified as a myopathic arthrogryposis multiplex congenita, rather than in the group of muscular dystrophies.

Arthrogryposis

[Congenital desproportion of various types of muscle fiber, with relative small size of type I fibers. Morphological documents on muscle biopsies in 3 members of the same family].

In two sisters with a neo-natal hypotonia, muscle biopsies demonstrated as main pathological feature a disproportion in size between the two types of muscle fibers defined according to their myofibrillar ATPase activity. Type I fiber mean diameter was at the lower limit of the normal values, and type II fibers were larger than normal. Their father's biopsy also showed an abnormal smallness of the type I fibers, with a bimodal distribution. By electron microscopy, the small type I fibers did not reveal any significant abnormality in children's biopsies. In father's biopsy, there was an abnormal degree of filamentary interchange between contiguous myofibrils and a few stacks of rods in the type I fibers. These three cases demonstrate the familiar character of the disorder. The relationship of this new entity with the other congenital myopathies is controversial, as a similar congenital fiber type disproportion, has been found in association with different ultrastructural changes. Several data favour an insufficient development of the type I fibers rather than an atrophying process. The mechanism of this "hypotrophy" remains unknown.

Adenosine Triphosphatases

X-linked recessive congenital muscle fiber hypotrophy with central nuclei: abnormalities of growth and adenylate cyclase in muscle tissue cultures.

Muscle cells in cultures established from biopsy specimens of two children with an infantile-fatal form of X-linked recessive muscle fiber smallness with central nuclei showed an unusual ability to proliferate through numerous passages. Ultrastructurally, the cultured muscle fibers appeared very immature even after several weeks. The nuclei were large, the number of ribosomes was greatly increased, the myofibrils remained unstriated, and glycogen was accumulated in large lakes. The plasmalemma bound concanavalin A, alpha-bungarotoxin, and ruthenium red normally, but with tannic acid it did not show the dark binding of mature fibers. Biochemically, in the cultured muscle fibers, beta-adrenergic receptors were quantitatively normal. The level of adenylate cyclase in membranes was less than in cultured normal muscle; this defect could be responsible for impaired control mechanisms resulting in the other abnormalities observed.

Adenylyl Cyclases

The syndrome of diabetic amyotrophy.

Changes in the electromyograms and motor nerve conduction velocities in 12 patients with diabetic amyotrophy suggested mild distal and moderate proximal neuropathy in the lower limbs. Histological and histochemical findings in the vastus medialis muscles were consistent with denervation. Electron microscopical examination of the vastus medialis muscles in 6 patients revealed myofibrillar degeneration. One patient had abnormal mitochondria and tubular aggregates. The basement membranes of the intramuscular capillaries were thickened in all but 1 patient. Histochemical staining of the myoneural junctions showed changes consistent with degeneration and regeneration. We conclude that diabetic amyotrophy is a distinct clinical entity and is secondary to metabolic derangement rather than diabetic microangiopathy.

Adult

Congenital fiber type disproportion in identical twins.

Eighteen-month-old identical twins with the muscle histological characteristics of congenital fiber type disproportion are reported. The fiber typing system of pH-dependent adenosine triphosphatase was used to analyze the size and percentage of type 1, 2A, and 2B fibers in muscle tissue obtained by needle biopsy. Both twins had significantly larger type 2 than type 1 fibers, with 2B fibers representing the largest type. One patient also had type 1 predominance at the expense of a reduction in 2B (2B deficiency). The probands as well as other family members had transient delayed motor development, macrocephaly, and normal intelligence. A biopsy obtained from 1 of these family members failed to demonstrate a similar histological abnormality. The disorder is nonprogressive in this family, as evidenced by minimal disability in the older members and gradual improvement in the probands.

Biopsy, Needle

Chronic neurogenic quadriceps amyotrophy.

Two patients with chronic neurogenic quadriceps amyotrophy are reported. A 61-year-old woman had symmetrical wasting and weakness of the quadriceps femoris of eight years' duration. A biopsy revealed neuropathic changes, and electromyograms showed neurogenic as well as myopathic patterns in the quadriceps and other muscles. A 29-year-old woman had long-standing wasting limited to the quadriceps and hip muscles. EMG and biopsy were compatible with neurogenic atrophy. She had a brother suffering from a more widespread and severe form of the disease. These cases suggest that chronic neurogenic quadriceps amyotrophy is a forme fruste of Kugelberg-Welander disease.

Adult

Nemaline (rod) myopathy: the need for histochemical evaluation of affected families.

Histochemical changes in the mother of a patient with nemaline myopathy were used to identify her as the gene carrier even though rod-bodies were not present in her muscle biopsy and she was not weak. The patient and her mother both had marked type I fiber predominance with large groups of type I fibers present. Histochemical changes known to occur in nemaline myopathy include smallness and predominance of type I fibers. Such changes support the concept that this disease may result from subtle defects in innervation since fiber types are determined by innervation. Although this disease is thought to be transmitted by autosomal dominant mode, lack of male-to-male transmission and a predominance of female cases in the literature suggest that this may be (1) an X-linked dominant, (2) a sex-influenced autosomal dominant, or (3) an autosomal dominant which is semilethal in males. The family described here is the first in which a presumably affected parent showed only the histochemical change without rod-bodies, thus emphasizing the importance of histochemical evaluation of relatives' biopsies for genetic counseling.

Biopsy

Centronuclear myopathy: possible central nervous system origin.

The authors describe a case of myopathy characterized physically by limb weakness, eyelid ptosis, voluntary and reflex paralysis of vertical movements of gaze, and loss of deep tendon reflexes; and morphologically by the abnormal presence of centrally located nuclei in muscle fibers and type 1 fiber hypotrophy. The establishment in this case study of two particular findings--the probably nuclear or supranuclear ophthalmoplegia and the apparently impaired nuclear migration from the center of the muscle fiber toward its periphery--supports the hypothesis of a neuromuscular disorder whose level of severity depends on the degree of difficulty in the nuclear migration itself. This would be linked to a reduction in central nervous system influence.

Adolescent

[Further investigations of insufficient stretching-closing mechanism of the terminal esophagus (author's transl)].

The anatomy of the closing mechanism of the terminal esophagus was studied in the dogs since this animal is frequently utilized for investigations of esophageal function. With the aid of a special method we have demonstrated a stretching-closing mechanism similar to that of the human subject. An operatively placed hiatus hernia with a tendency to reflux shows the expected reaction of the muscular screw mechanism. This insufficient stretching-closing mechanism is similar to an insufficient "ring sphincter". The reconstruction of the closing mechanism by means of "stretching and gastropexie" which has proven successful in practice is discussed.

Animals

Weakness in myotonic syndromes.

Muscle weakness occurs in a number of myotonic syndromes, including those in which muscle bulk is preserved. The possible causes of muscle weakness may be considered in terms of the different stages of the electromechanical activation process and defects in the contractile machinery. In individual myotonic disorders the ability to identify the origin of the muscle weakness (whether neurogenic or myogenic) and the functional level at which the defect occurs would assist the choice of rational treatment.

Action Potentials

[Influence of the Benzodiazepine-derivative Ro 06-9098/000 on choreo-athetotic syndromes (author's transl)].

Five patients suffering from choreo-athetotic syndromes of different genesis were treated with the benzodiazepine-derivative Ro 06-9098/000 (7-Nitro-1(methylmethoxy)-1,3-dihydro-5-phenyl-2 H-1,4-benzodiazepin-2-one). The existing hyperkinesias could be well influenced in four cases of male patients, sufficiently in one case of a female patient. The sedative effect, accompanied by a muscle hypotonia appearing simultaneously under the medication, did not represent and essential limiting factors at the chosen dose of 5--20 mg/die. The observed successes in therapy point at the result and effect of benzodiazepine derivatives on extra-pyramidalmotoric hyperkinesias which got little attention until now.

Adult

Muscle biopsy in hypotonic schizophrenic children: a preliminary report.

Two hypotonic boys, aged 7 years, 3 months and 7 yers, 7 months, who possessed sufficient speech to demonstrate a severe thought disorder and who differed markedly in their activity levels, were subjected to a biopsy of the quadriceps muscle. The biopsies revealed atrophy of type 2 muscle fibers, as well as variability in the size of these fibers. The findings could be compatible with a denervation phenomenon.

Adenosine Triphosphatases

Tetrahydrobiopterin therapy of atypical phenylketonuria due to defective dihydrobiopterin biosynthesis.

A patient with atypical phenylketonuria (defective BH2 synthesis), detected at age 6 months because of severe muscle hypotonia and serum phenylalanine of 20 mg/100 ml, had normal activities of phenylalanine-4-hydroxylase and DHPR in liver biopsy, but only 2% activity in the phenylalanine-4-hyroxylase in vivo test using deuterated phenylalanine. After IV administration of 2.5 mg/kg chemically pure tetrahydrobiopterin bishydrochloride (BH4 . 2HCl), serum phenylalanine decreased from 20.4 to 2.1 mg/100 ml within 3 hours. Administration of 25 mg BH4 . HCl and 100 mg ascorbic acid through a gastric tube decrease; serum phenylalanine from 13.7 to less than 1.6 mg/100 ml within 3 hours and it remained less than 2 mg/100 ml for 2 days.

Biopterins

Congenital fibre type disproportion myopathy. A histological diagnosis with an uncertain clinical outlook.

Nine children with congenital fibre type disproportion (CFTD) are described. Their muscle biopsies contained type 1 fibres which were smaller than the largest type 2 fibres by at least 13.5%. Attention is drawn to the variable natural history of this disorder which generally carries a good prognosis but may sometimes be associated with fatal respiratory problems. For important therapeutic, genetic, and prognostic reasons CFTD must be distinguished from other conditions with similar histochemical or clinical features.

Biopsy